Senior Onset is typically the result of the normal aging of the immune system and is of little interest to me. Young Onset, however, is another matter. It begins with fetal exposure to the waste products of maternal bacterial infection (the toxin lipopolysaccharide or LPS in particular). While the fetal defenses are normally up to their task, there are occasional breeches. If these happen to occur at times of critical development the result can be a fetal immune system that is hypervigilant and which poses a danger to itself.

This is a lot to swallow at one sitting, but it is true. And it is all drawn from the work of "real" scientists and their peer reviewed work. I am going to quote liberally from that work and try to fill in the messy parts afterward.
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A Matter of Balance
Thus, exposure to the bacteriotoxin, lipopolysaccharide (LPS) during a critical developmental window in rats, leads to the birth of animals with fewer than normal dopamine (DA) neurons. This DA neuron loss is apparently permanent as it is still present in 16 months old animals (the longest period studied to date). Moreover, the loss of DA neurons seen in these animals increases with age thereby mimicking the progressive pattern of cell loss seen in human PD. (Carvey 2003)


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One is a reduced density of dopaminergic neurons in the substantia nigra and another is hypersensitivity to further exposure – the system is “primed”. Future exposure to LPS, particularly after the changes of puberty, will trigger a greater reaction whose magnitude will vary with individual sensitivity.

Sensitivity to LPS is genetically determined, varying considerably among different species. The sensitivity of normal animals (mice) to endotoxin may be enhanced considerably under different experimental conditions that include treatment with live (infection) or killed Gram-negative and -positive bacteria. (Fruedenberg 1993)

We conclude that prenatal exposure to LPS produces a long-lived THir cell loss that is accompanied by an inflammatory state that leads to further DA neuron loss following subsequent neurotoxin exposure. The results suggest that individuals exposed to LPS prenatally, as might occur had their mother had bacterial vaginosis, would be at increased risk for Parkinson’s disease. (Carvey 2004)

Thus, this disrupted immune system can lead to chronic inflammation and microglial activation with elevated levels of cytokines and related pro-inflammatory chemicals leading to “cell death.

The twin roots (immune and endocrine) of Parkinson’s Disease reaching back to the earliest moments of existence represent the extreme of a spectrum of causal scenarios and produce the earliest onset of symptoms. The two arise together and interact to produce the disorder by means of a self-perpetuating immune-endocrine reaction.